Receptor tyrosine kinase plays a key role various aspects of tumor such as tumor genesis and development, invasion and metastasis, and drug resistance because of the activation of its abnormal expression or gene mutation. It has become an important target for anti-tumor drug research and development. Among them, fibroblast growth factor receptors (FGFRs) are important members of the receptor tyrosine kinase family, mainly including four subtypes, FGFR1, FGFR2, FGFR3 and FGFR4. The ligand thereof is fibroblast growth factors (FGFs). Because of gene amplification, mutation, fusion or ligand induction and other reasons, the various members of FGFRs are continuously activated, inducing tumor cell proliferation, invasion, migration, promoting angiogenesis and promoting the genesis and development of tumor. FGFRs are highly expressed and abnormally activated in a variety of tumors, and are closely associated with poor prognosis in patients such as those with non-small cell lung cancer, breast cancer, stomach cancer, bladder cancer, endometrial cancer, prostate cancer, cervical cancer, colon cancer, esophageal cancer, glioblastoma, myeloma, rhabdomyosarcoma and the like. Studies have shown that FGFR1 amplification accounts for 20% of non-small cell lung cancer squamous cell carcinoma, and the studies of in vitro proliferation and signaling pathway of the lung cancer cell strains with FGFR1 proliferation have shown that FGFR selective inhibitors can effectively inhibit the activation of FGFR1 signaling pathway and cell proliferation. In breast cancer, the amplification of the chromosome region (8p11-12) where FGFR1 locates makes up approximately 10% of the ER-positive patients, and is associated with high expression of FGFR1 mRNA and poor prognosis of patients. FGFR2 gene amplification or mutation results in the abnormal activation of the FGFR2 signaling pathway, which is mainly associated with gastric cancer, triple negative breast cancer, endometrial cancer and the like. The amplification rate of FGFR2 in gastric cancer tissue is 5%-10%. Analysis of 313 cases of gastric cancer showed that the amplification of FGFR2 was significantly associated with tumor size, local infiltration, lymph node metastasis and distant metastasis, and furthermore, the gastric cancers with FGFR2-amplification are usually progressive tumor with poor prognosis, and the overall survival rate of patients is relatively low. FGFR2 amplification accounted for 4% of the refractory triple-negative breast cancers. Endometrial cancer is a common gynecological reproductive tract tumor, FGFR2 mutation accounts for about 12% of endometrial cancer. In non-invasive bladder cancers, FGFR3 mutations accounts for 50%-60%, and in invasive bladder cancers, FGFR3 mutations accounts for 10%-15%. The gene rearrangement of FGFR3t (4; 14) (p16.3; q32) accounts for 15-20% of multiple myeloma. Meanwhile, various subtypes of FGFR and the ligands thereof (FGFs), such as FGFR2, FGFR3, FGFR4, FGF19, FGF2, FGF5, FGF8, FGF9, have shown aberrant expression and activation in liver cancer. Numerous preclinical and clinical studies have shown the importance of FGF/FGFR axis abnormal activation in liver cancer. It can not be ignored that abnormal activation of the FGF/FGFR axis is closely related to the drug-resistance to EGFR inhibitors, neovascularization inhibitors, and endocrine therapy. Therefore, development of the inhibitors targeting FGFR has become a hot spot in the field of anticancer drug research.